p16基因导入致人乳腺癌MCF-7细胞端区缩短及细胞周期阻滞  

Telomere Shortening and Cell Cycle Arrest Induced by p16 Gene Introduction in Human Breast Cancer MCF-7 Cells

作　　者：段建明[1] 刘平湖[1] 张宗玉[1] 童坦君[1] 

机构地区：[1]北京医科大学生物化学与分子生物学系,北京100083

出　　处：《中国生物化学与分子生物学报》2000年第1期124-127,共4页Chinese Journal of Biochemistry and Molecular Biology

基　　金：国家自然科学基金!重点项目资助课题 ( 3 993 0 170 )

摘　　要：为进一步探讨 p1 6基因在抗肿瘤及细胞衰老中的作用 ,以脂质体介导的方法 ,将重组的含全长 p1 6c DNA的逆转录病毒载体导入人乳腺癌 MCF- 7细胞 ,获得稳定整合有效表达 .检测其对MCF- 7细胞的端区长度、细胞形态、增殖特性及细胞周期的影响 .结果显示 :导入 p1 6c DNA后的MCF- 7细胞端区长度明显缩短、增殖减慢 ,细胞周期阻滞于 G1期 .由此推测 ,野生型 p1 6基因可能通过诱导端区缩短效应及抑制细胞增殖从而抑制肿瘤和启动细胞衰老 .To investigate the roles of p16 in tumor suppression and cell senescence.p16 cDNA retroviral vector was introduced into MCF 7 cells by liposome mediated transfection.It was stably integrated into the genomic DNA and was expressed effectively.Then the effects of p16 on the telomeric length,cell morphology,proliferation and cell cycle of MCF 7 cells were measured.The MCF 7 cell transfected with p16 cDNA showed significantly telomeric shortening,proliferative restraint and G 1 cell cycle arrest compared with the control cells.All the results suggest that the wild type p16 may play an important role in tumor suppression and initiate cell senescence beginning by the mechanism of inducing cell telomeric shortening and growth arrest.

关 键 词：P16 肿瘤抑制 细胞衰老 细胞周期 MCF-7细胞端区 

分 类 号：R730.5[医药卫生—肿瘤] Q78[医药卫生—临床医学]